In 2011 suPAR, the soluble urokinase-type plasminogen activation receptor (free PMC pdf review), arrived in the literature on a wave of hype. Serum suPAR levels were elevated in two thirds of patients with FSGS. More significantly, this was purported to be specific for FSGS. A pathogenic role for suPAR was supported by three mouse models. Since the 2011 paper, as to often occurs, the hype was replaced by controversy as verification of these findings was difficult.

At #KidneyWk 2015, suPAR shed its FSGS etiology origin story and was reborn as a CKD biomarker.

Methods

This was a prospective study that measured plasma suPAR in 3,683 patients enrolled in a biobank. They followed renal function at subsequent visits in 2,292 and used diverse analytical techniques to assess the relationship between suPAR, baseline eGFR, change in eGFR, and the development of CKD.

Results

Splitting serum suPAR into two groups showed that higher suPAR at baseline was associated with numerous traditional CKD risk factors

Decline in eGFR was greater in patients with higher suPAR and this was independent of race and diabetes but not of baseline eGFR

Patients with a normal eGFR at baseline had the largest suPAR related decline in renal function

24% of the cohort developed CKD and this incidence of CKD was associated with a higher suPAR level at baseline almost in a “dose dependent” manner

Conclusion & Discussion

elevated plasma suPAR levels were associated with incident chronic kidney disease and a more rapid decline in the eGFR in persons with normal kidney function at baseline.

Questions:

Did the study’s lack of a decent quantification of proteinuria mean that suPAR is just a novel replacement for albuminuria measurement?

Why were there no calculations of positive and negative predictive values or repeat suPAR measurements?